The AGGF1 Knockout LoVo Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population engineered from the human LoVo colorectal adenocarcinoma cell line. This product provides a heterogeneous loss-of-function model with targeted disruption of the AGGF1 gene, which encodes an angiogenic factor implicated in vascular development and tumor angiogenesis. The polyclonal format preserves the natural genetic diversity arising from CRISPR-mediated gene disruption across the cell population, making it a versatile tool for studying AGGF1-dependent processes in a cancer-relevant context without clonal selection bias.
LoVo cells were originally isolated from a supraclavicular lymph node metastasis of a Dukes?? type C colorectal adenocarcinoma and are characterized by an epithelial morphology. Widely employed as a model system for colorectal cancer, these cells exhibit robust in vitro growth and are extensively used to investigate tumor progression, metastasis, and the tumor microenvironment. Their genetic background and metastatic origin make them particularly suitable for examining angiogenesis-related pathways that support tumor growth and dissemination.
AGGF1 functions as a pro-angiogenic factor that stimulates endothelial cell proliferation and tube formation, processes essential for new blood vessel formation. It is transcriptionally upregulated by hypoxia-inducible factor 1-alpha (HIF-1??) under low-oxygen conditions and acts downstream of various growth factors. AGGF1 promotes the expression of vascular endothelial growth factor (VEGF) and engages in signaling crosstalk with VEGF receptors (VEGFR) and the Notch pathway, potentially interacting with Notch1 and its ligand Dll4. This network integrates into broader cascades such as the PI3K/AKT pathway, linking AGGF1 to endothelial cell survival and migration. The protein can also self-associate, suggesting a mode of regulation through oligomerization.
In the LoVo colorectal adenocarcinoma background, AGGF1 knockout enables dissection of tumor-derived angiogenic signaling. LoVo cells are known to secrete angiogenic factors that remodel the vascular niche; disruption of AGGF1 in these cells offers a physiologically relevant platform to assess its contribution to paracrine activation of endothelial cells. This model is therefore valuable for exploring how colorectal cancer cells modulate the vascular system and for identifying vulnerabilities in tumor-driven angiogenesis without interference from stromal AGGF1 sources.
Key applications include performing tube formation assays to evaluate endothelial cell morphogenesis, endothelial cell proliferation and migration assays to quantify angiogenic potential, and co-culture experiments to study tumor-endothelial interactions. Downstream molecular analyses can be conducted via Western blotting, RT-qPCR, and immunofluorescence to characterize signaling alterations in the VEGF, Notch, and PI3K/AKT pathways. This AGGF1 knockout tool supports investigations into colorectal cancer progression, vascular malformation mechanisms, and the hypoxic tumor microenvironment. For further technical information, please contact Ascent Research.
